To investigate whether energy derived from glycolytic and oxidative metabolism are preferentially used for different functions in heart, tension, intracellular potential, and extracellular [K+] and pH (using triple barrel K/pH electrodes, tip diameter 0.5 mm) were monitored in isolated arterially perfused rabbit interventricular septa during exposure to hypoxia and metabolic inhibitors. Myocardial content of high energy phosphates, lactate, and glycogen were determined under the same conditions. Inhibiting oxidative metabolism with hypoxia, dinitrophenol (10-s M), or Na-azide (10-3 M) caused marked suppression of tension (by 73±5, 65±8, and 50±14%, respectively) and a small increase in [K+]> (0.8±0.4, 0.5±0.25, and 0.4±0.2 mM, respectively) after 10 min. Inhibiting glycolysis with iodoacetate (IAA) (10-3 M) had a much smaller suppressant effect on tension (28±24%) but markedly increased IK'io accumulation (by 1.8±1.1 mM) at 10 min. These differences, when IAA was compared individually to the other interventions, were highly significant. The shortening of action potential duration was not significantly different for the four interventions. pHO increased slightly during IAA (+0.04-+0.06 U) and fell during the other interventions (-0.10--0.16 U), but this did not account for the differences in [K+]J accumulation and tension between inhibition of glycolytic vs. oxidative metabolism. Except for hypoxia, total cellular content of high energy phosphates was not significantly depressed under the various conditions. This data suggests that energy from glycolysis is preferentially used to support sarcolemmal function (as manifested by K+ loss), whereas oxidatively derived energy preferentially supports contractile function.

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To investigate the contribution of acidosis to contractile dysfunction during early myocardial ischemia, miniature intramyocardial pH electrodes (0.2 mm tip diam) were used to correlate changes in extracellular pH (pHo) with tension in the isolated arterially perfused rabbit interventricular septum. A number of findings argue against acidosis as the major cause of contractile failure during early ischemia. During hypoxia without glucose present, the rate and pattern of tension decline was very similar to total ischemia, suggesting that a common mechanism is involved. Throughout the initial period in which tension declined by 50%, however, pHo increased in the six of eight preparations during hypoxia without glucose. During hypoxia with glucose present, tension fell less rapidly than during hypoxia without glucose despite a significantly greater fall in pHo in the former case. The maximal rate of relaxation (-dT/dt) was markedly more sensitive to ischemia, hypoxia, or exposure to inhibitors of aerobic metabolism (2,4-dinitrophenol and Na azide) than the maximal rate of force development (+dT/dt). In contrast, +dT/dt and -dT/dt decreased almost symmetrically during exposure to respiratory acidosis. During ischemia, the change in pHo associated with 50% reduction in tension was 0.11 +/- 0.04 units. During respiratory acidosis, this value was 0.45 +/- 0.02 units. From these observations we concluded that acidosis is unlikely to be a major factor in the early decline of tension during ischemia.

Objectives: To determine symptomatology, clinical class, and topographic patterns of varicose veins in a consecutive series of patients with venous complaints. Methods: We performed clinical examination and duplex scanning of 498 lower limbs in 317 patients with obvious varicose veins for whom no previous treatment had been undertaken. Results: Classes of chronic venous insufficiency (CVI) in 498 legs: grade 0: 117 (23.5%); gr 1: 310 (62.2%); gr 2: 47 (9.4%); gr 3: 24 (4.8%). Duplex-detected venous reflux was found in the greater saphenous vein territory (junction or trunk or related perforator or main tributary) in 423 limbs (85.3%) the sapheno-femoral junction was incompetent in only 342 legs (68.7%). Reflux was found in the lesser saphenous vein territory in 100 limbs (20.1%) and in sapheno-popliteal junction in 92 (18.5%). Strictly non saphenous origin of varicosities was found in 31 limbs (6.2%). Deep venous incompetence was found in 48 legs (9.6%). Conclusions: These findings yield data on the distribution and occurence of lower limbs venous lesions in patients with varicose disease.

To investigate the factors determining the rate of H+ accumulation during early ischemia, miniature intramyocardial pH electrodes (tip diam 0.2-0.5 mm) were used to record extracellular pH (pHo) in the isolated arterially perfused rabbit interventricular septum. Changes in pHo and the rate of fall of tension during global ischemia were compared under control conditions (37 degrees C, heart rate 75 beats/min) and after exposure to the following interventions: reduced heart rate (36 beats/min), hypothermia (27 degrees C), verapamil (0.5 microM), reduced extracellular Ca2+ concentration [( Ca2+]o 0.5 mM), norepinephrine (0.5 microM) in normal and catecholamine-depleted preparations, norepinephrine and reduced [Ca2+]o, and theophylline (4 mM). Under control conditions pHo declined by 0.61-0.73 pH units after 10 min of ischemia. The negative inotropic interventions and reduced temperature significantly decreased [H+]o accumulation during ischemia. Positive inotropic interventions did not affect the rate of [H+]o accumulation during ischemia except in reserpinized preparations. All of the interventions except for reduced temperature significantly altered the relationship between tension and pHo during ischemia.